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本文引用的文献

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Salmonella--the ultimate insider. Salmonella virulence factors that modulate intracellular survival.沙门氏菌——终极内奸。调节细胞内存活的沙门氏菌毒力因子。
Cell Microbiol. 2009 Nov;11(11):1579-86. doi: 10.1111/j.1462-5822.2009.01368.x. Epub 2009 Sep 23.
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Ubiquitination of the bacterial inositol phosphatase, SopB, regulates its biological activity at the plasma membrane.细菌肌醇磷酸酶 SopB 的泛素化调节了其在质膜上的生物学活性。
Cell Microbiol. 2009 Nov;11(11):1652-70. doi: 10.1111/j.1462-5822.2009.01356.x. Epub 2009 Jul 13.
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Respective roles of culturable and viable-but-nonculturable cells in the heterogeneity of Salmonella enterica serovar typhimurium invasiveness.可培养细胞与活的但不可培养细胞在肠炎沙门氏菌鼠伤寒血清型侵袭异质性中的各自作用。
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Diversification of a Salmonella virulence protein function by ubiquitin-dependent differential localization.通过泛素依赖性差异定位实现沙门氏菌毒力蛋白功能的多样化。
Cell. 2009 Apr 17;137(2):283-94. doi: 10.1016/j.cell.2009.01.056.
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GFP plasmid-induced defects in Salmonella invasion depend on plasmid architecture, not protein expression.绿色荧光蛋白质粒诱导的沙门氏菌侵袭缺陷取决于质粒结构,而非蛋白质表达。
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Salmonella takes control: effector-driven manipulation of the host.沙门氏菌掌控全局:效应蛋白驱动的宿主操控
Curr Opin Microbiol. 2009 Feb;12(1):117-24. doi: 10.1016/j.mib.2008.12.001. Epub 2009 Jan 20.
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Gene set analyses for interpreting microarray experiments on prokaryotic organisms.用于解释原核生物微阵列实验的基因集分析。
BMC Bioinformatics. 2008 Nov 5;9:469. doi: 10.1186/1471-2105-9-469.
8
Interaction of Salmonella enterica serovar Typhi with cultured epithelial cells: roles of surface structures in adhesion and invasion.肠炎沙门氏菌伤寒血清型与培养的上皮细胞的相互作用:表面结构在黏附和侵袭中的作用
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9
FliZ Is a posttranslational activator of FlhD4C2-dependent flagellar gene expression.FliZ是FlhD4C2依赖性鞭毛基因表达的翻译后激活因子。
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10
Do Salmonella carry spare tyres?沙门氏菌携带备用基因吗?
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不同生长条件下诱导沙门氏菌致病性岛 1 可影响沙门氏菌与宿主细胞的体外相互作用。

Induction of Salmonella pathogenicity island 1 under different growth conditions can affect Salmonella-host cell interactions in vitro.

机构信息

Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA.

Genomics Unit, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA.

出版信息

Microbiology (Reading). 2010 Apr;156(Pt 4):1120-1133. doi: 10.1099/mic.0.032896-0. Epub 2009 Dec 24.

DOI:10.1099/mic.0.032896-0
PMID:20035008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2848694/
Abstract

Salmonella invade non-phagocytic cells by inducing massive actin rearrangements, resulting in membrane ruffle formation and phagocytosis of the bacteria. This process is mediated by a cohort of effector proteins translocated into the host cell by type III secretion system 1, which is encoded by genes in the Salmonella pathogenicity island (SPI) 1 regulon. This network is precisely regulated and must be induced outside of host cells. In vitro invasive Salmonella are prepared by growth in synthetic media although the details vary. Here, we show that culture conditions affect the frequency, and therefore invasion efficiency, of SPI1-induced bacteria and also can affect the ability of Salmonella to adapt to its intracellular niche following invasion. Aerobically grown late-exponential-phase bacteria were more invasive and this was associated with a greater frequency of SPI1-induced, motile bacteria, as revealed by single-cell analysis of gene expression. Culture conditions also affected the ability of Salmonella to adapt to the intracellular environment, since they caused marked differences in intracellular replication. These findings show that induction of SPI1 under different pre-invasion growth conditions can affect the ability of Salmonella to interact with eukaryotic host cells.

摘要

沙门氏菌通过诱导大量肌动蛋白重排来侵入非吞噬细胞,导致膜皱襞形成和细菌的吞噬作用。这个过程由一群效应蛋白介导,它们通过 III 型分泌系统 1 被转运到宿主细胞中,III 型分泌系统 1 由沙门氏菌致病性岛(SPI)1 调控子中的基因编码。这个网络受到精确的调控,必须在宿主细胞外诱导。尽管细节有所不同,但在体外侵袭性沙门氏菌是通过在合成培养基中生长来制备的。在这里,我们表明培养条件会影响 SPI1 诱导细菌的频率,从而影响入侵效率,并且还可以影响沙门氏菌在入侵后适应其细胞内小生境的能力。好氧生长的晚期指数期细菌的侵袭性更强,这与通过单细胞基因表达分析揭示的 SPI1 诱导的运动细菌的更高频率有关。培养条件还影响了沙门氏菌适应细胞内环境的能力,因为它们导致细胞内复制的明显差异。这些发现表明,在不同的入侵前生长条件下诱导 SPI1 可以影响沙门氏菌与真核宿主细胞相互作用的能力。